Fructose Flashcards

1
Q

Historical perspective of fructose intake

A
  • ever increasing sugar intake
  • change in the type we consuming - more HFCS
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2
Q

How do different sugars differ in sweetness and GI?

A

very sweet but low GI

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3
Q

Why is fructose often used in food industry?

A

sweeter, cheaper, good consistency

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4
Q

Is fructose the optimal low GI sweetener?

A

No, it has a different metabolic fate from glucose and contributes little to energy

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5
Q

metabolic fate of fructose

A

fructose breakdown uses ATP to make fructose 1 phosphate and process makes uric acid
* F1P can be further broken to make pyruvate with more production of urin acid or can be converted to TAG

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6
Q

How does F1P effect glucose?

A
  • stimulates glycolysis
  • stimulates glycogenesis and inhibits glycogenolysis
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7
Q

Proposed effects of fructose on hepatic lipid metabolism

A
  • Increases TG packaged into the VLDL
  • contributes to hepatic denovo lipogenesis
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8
Q

How fructose and glucose differ with effects on brain regions involved with appetite and reward?

A

fructose provokes feeding (promotes less satiety hormones) and glucose promotes greater satiety

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9
Q

What is the difference in metabolic and hormonal response between fructose and glucose?

A

Fructose drink results in a lower insulin response, lower GLP-1 response and more lactate.
* shows spill over in the 2 paths

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10
Q

What enzyme first breaks down fructose

A

fructokinase
* it is not sensed by glucokinase

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11
Q

Does glucose or fructose produce more satiety?

A
  • glucose leads to greater fullness and satiety
  • fructose does not lead to fullness likely due to less insulin and GLP-1 and people will often eat more
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12
Q

How do fructose and glucose differ in brain activation?

A
  • more activation with glucose in the hypothalamus, thalamus, putamen, caudal
  • fructose has only a small activation in the hypothalamus and thalamus
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13
Q

What might control sugar seeking behaviour?

A

glucose responsive neurons expressing GLUT2 in the paraventricular thalamus (PVN)
* may control sugar overconsumption in obesity and T2D
* Also expressed in the beta cells

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14
Q

What happens with loss of neuronal GLUT2?

A

increases glucose seeking behavior
* Eat more food wtihout GLUT2 in the brain

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15
Q

When are GLUT 2 expressing neurons activated?

A

They are activated, or make you go seek food, at kow glucose
* Once you consume glucose they are deactivated

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16
Q

How do GLUT 2 expressing neurons respond to fructose?

A

Do not respond to fructose so still activated after a fructose meal (still seeking food)

17
Q

What has confirmed the role of GLUT2 neurons in glucose seeking behaviour?

A

Optogenetics
* a biological technique to control the activity of neurons or other cell types with light.
* increases CBF

18
Q

Summary of fructose studies

A
19
Q

First time fructose was linked with diabetes

A

research article 1977 - diabetes induced by a high fructose diet

20
Q

How might fructose effect the gut microbiome?

A

Fructose has the potential to affect “gut health”, including barrier deterioration, dysbiosis, and the production of active metabolites (FA, glycerate).
* fructose can cause microbiome changes to make SCFA
* increased permability of the endothelium
* endotoxemia - microbiome and their products can enter the body

21
Q

How does fructose consumption compare to an already bad diet?

A

glycerate from intestinal fructose metabolisms induces islet cell damage and glucose intolerance
* glycerate is toxic to islets

22
Q

How does a HF diet compare to CD?

A

The HFD resulted in greater levels of glycerate both in the portal vein and systemic circulation

23
Q

What happened with rats treated with glycerate?

A

rats treated with glycerate have degraded islets and impaired fasting glucose

24
Q

Where is fructose metabolized?

A

Fructose was thought to be metabolized predominantly in the liver, but evidence is emerging that it is also metabolized in the small intestine.